Body Defenses & Immunity: But If Skin Is Moist, Not Cleaned Frequently Enough

Body Defenses & Immunity
the immune system is a functional system rather

immunity = resistance to disease than a system with discrete organs
! parts of many organs contribute to body
the immune system provides defense against all the defense
microorganisms and toxic cells to which we are almost all organs in body play some role in
exposed immunity
! without it we would not survive till ! dispersed chemicals, cells and tissues
adulthood
! dispersal and transport via circulatory and
our body has many ways to prevent or to slow lymphatic systems
infections
two major kinds of mechanisms that protect the
Individual Susceptibilities body:
Many factors not directly related to our “immune 1. Nonspecific Immunity

system” affect an individual’s overall ability to
resist infections: an innate reaction that acts as a general
response against all kinds of pathogens
eg. Genetics: human diseases, zoonoses, etc
eg. Age: mainly an immune response

a. physical and chemical barriers
b. internal cells and chemicals
eg. Health: eg. protein deficiency ! less phagocytic activity
eg. stress ! lower resistance to disease 2. Specific Immunity
eg. Hormones: eg. cortisone (a glucocorticoid)
reduces inflammatory response an adaptive system that fights specific
individual pathogens in customized ways
eg. Microbiome: activate our immune system and affect our
susceptability to diseases
The Immune System

Human Anatomy & Physiology: Body Defense & Immunity; Ziser Lecture Notes, 2014.4 1 Human Anatomy & Physiology: Body Defense & Immunity; Ziser Lecture Notes, 2014.4 2
Nonspecific Immunity a. consists of multiple layers of tightly packed

dead cells filled with waxy keratin
nonspecific mechanisms for protecting the body can
be visualized as offering two distinct levels of b. shed regularly to prevent buildup of bacterial
protection communities
! physical & chemical barriers that work to c. sebaceous glands provides protective film
prevent entry of pathogens over skin
! internal cells & chemicals that attempt to d. acidity of skin secretions ('acid mantle')
remove pathogens if they get past the barriers inhibit bacterial & fungal growth
Physical Barriers e. skin also contains bacteriocidal chemicals

but if skin is moist, not cleaned frequently enough
1st major level of protection from invasion and
infection !may permit yeasts and fungi already present
to become a problem
nonspecific – treats all potential pathogens the same f. Langerhans cells ( & Granstein cells) ! serve as
way antigen presenting cells
attempt to prevent entry of pathogens into body they expose skin antigens to T cells
1. Intact Skin 2. Mucous Membranes
skin is rarely, if ever, penetrated while intact line all systems that open to outside of body
only a few bacteria and parasitic worms (cercariae) can do a. secretes mucus
this
thick, sticky, traps pathogens
if skin is broken: staphs and streps are most likely to get in
b. in the nose nasal hairs help trap pathogens
c. many mucus membranes have cilia low flow ! bladder infection
in resp system move mucus out of system acidity also inhibits bacterial growth
(‘ciliary escalator’ ! 1-3 cm/hr) h. vaginal secretions

coughing and sneezing speed up process flushing and trapping pathogens in mucous
d. stomach lining secretes gastric juices acidity also inhibits bacterial growth
contains HCl and enzymes; highly acidic (pH~1.2-3.0) but: some pathogens thrive in moisture and if they
occur in large enough numbers they are able to
kill and dissolve most bacteria and toxins penetrate eg. Treponema
except S. aureus and C. botulinum
Internal Cells & Chemicals
but: Helicobacter pylori neutralizes acids to grow in
stomach
may cause gastritis or ulcers 1. blood has nonspecific, antimicrobial chemicals that
help to fight invaders:
e. eye is protected by lacrimal apparatus
eg. transferrins – bind to Fe to inhibit bacterial growth
continual blinking flushes and wipes away
pathogens 2. Simple Phagocytosis
lysozyme in tears kills and dissolves some bacteria many WBC’s travel through blood and tissues and
(most G+ and some G- bacteria)
gobble up bacteria and foreign material
(lysozyme also found in sweat, saliva, and nasal
secretions)
mostly neutrophils and macrophages (formed from
monocytes)
f. saliva in mouth allows continual flushing of
bacteria to stomach migrate to area of infection
lysozyme kills and dissolves some bacteria monocytes enlarge on way to become
macrophages
g. urine provides continual flushing of bacteria
entering urethra
engulf and destroy circulating pathogens
especially bacteria takes 10-30 minutes to kill most bacteria

enzymes:
lysozyme ! hydrolyzes peptidoglycan of cell
some macrophages are “fixed macrophages” that wall
lipases, proteases, ribonucleases !
screen blood as it passes by hydrolyzes other cellular components
some enzymes also produce toxic oxygen
! esp in liver, bronchial tubes of lungs, nervous products: eg. O2-, H2O2, OH-
system, , spleen, lymph nodes, bone marrow
peritoneal cavity residual body discharges wastes
[referred to as the reticuloendothelial system] not all microorganisms are killed once phagocytized
mechanism of phagocytosis: eg. Staph and Actinobacillus actually produce

toxins that kill phagocytes
a. Chemotaxis
eg. Chlamydia, Shigella, Mycobacterium,
chemical attraction to invaders, microbial products, Leishmania (protozoan), and Plasmodium
components of WBC’s or damaged cells can survive inside phagocyte
! they can prevent fusion of lysozome
b. Adherence
eg. other microbes can remain dormant for
attachment to surface of foreign material months
may be hampered by capsules (eg. S. pneumonia, H.
Influenza) or M proteins (eg. S. pyogenes) phagocytosis also plays a role in specific immunity
! must trap them against rough surface
(eg. blood vessel wall, clot, etc)
3. eosinophils
also can be more readily phagocytized if 1st coated
with certain plasma proteins that promote can produce toxins and are most active against
attachment (=opsonization) parasitc worms
c. Ingestion
4. Natural Killer Cells
plasma membrane of phagocyte extends around
microorganism or cell
the “pit bulls” of the defense system
d. Digestion
another kind of WBC; not phagocytic
forms food vacuole inside WBC
fuses with lysozomes
police the body in blood and lymph
promote cell lysis of virus infected cells or a. Vasodilation and Increased Permeability
cancer cells
damaged tissues release histamines and kinins
5. Inflammatory Response blood vessels dilate in area of damage
larger response that prevents spread of infection !increased blood flow to area
from localized area causes swelling (edema), redness and heat
damage to body’s tissues causes: this allows defensive chemicals and clotting factors and cells
to move to the area
redness, pain, heat and swelling clot forms around area to prevent spread of infection
sometimes loss of function b. Phagocyte Migration and Phagocytosis

within an hour phagocytes begin to accumulate at the site
overall, has beneficial effect:
as the flow of blood decreases, phagocytes stick to lining of
a. destroys injuring agent blood vessels then squeeze out into tissue spaces
chemical attractants, eg. kinins, draw WBC’s to site

b. removes it and its byproducts or limits its
effects neutrophils arrive first, monocytes predominate during later
stages
c. repairs or replaces damaged tissues as WBC’s die ! pus accumulates
occurs in three major stages: c. Tissue Repair

cant be completed until all harmful substances have been
a. vasodilation removed or neutralized
b. phagocyte migration and phagocytosis 6. Fever
c. tissue repair systemic rather than local response

eg interferon
involves coordinated autonomic, neuroendorine
and behavioral response very high temperatures (>40º C) may be life
threatening
used by all vertebrates as acute phase reaction to
immune challenge 7. Complement Reactions
hypothalamic thermostat is reset usually to 1-4 foreign substance may trigger cascade
degrees above normal which activates complement proteins
=complement fixation
eg. 102.2 ºF
produced by pyrogens secreted by macrophages ~5% of all blood proteins (20 different ones) are
when exposed to certain pathogens complement proteins
fever symptoms: they can operate nonspecifically or specifically

blood vessels constrict
metabolism increases
shivering helps maintain high temp complement proteins formed from liver cells, lymphocytes,
skin remains cold – chills monocytes
slight increase in temperature: trigger a cascade reaction (inactive! active)

! initiation
a. inhibits growth of some pathogens ! amplification
! effects
b. speed metabolism
for repair of body cells complement fixation can cause any of the
and to enhance phagocytosis following effects:
a. cell lysis (cytolysis)
c. cause liver and spleen to store zinc and
iron; both are nutrients needed by membrane attack complex forms “transmembrane
bacteria channels”
!digests a hole in bacterial cell, killing it

d. intensifies effects of other chemicals
b. opsonization
effective for only short periods
makes pathogens stickier and easier for the leukocytes
to phagocytize
! good for acute, short term infections
c. enhances infllammatory response eg. colds, influenza
helps trigger release of histamine and chemical
interferon is now produced in quantity by recombinant DNA
attractants for WBC’s
technology
the effects of complement activation are short has only very limited effects on cancer cells
lived
! they are quickly destroyed high doses have side effects:
fatigue, fever, chills, joint pain, seizures
malfunctions of system may result in some hypersensitivity
experimentally used to treat HIV, Hepatitis, genital herpes,
disorders
influenza, common cold
8. Interferon might work better with other agents in combination
antiviral chemical secreted by infected cells
they are host cell specific, not virus specific
! different tissues in same host produce

different interferons
all interferons are small proteins

stable at low pH
heat resistant
produced by infected cells and spread to

uninfected cells
! stimulate synthesis of antiviral proteins that disrupt
various stages of viral multiplication
Specific Immunity on its size and complexity
functionally, the third line of defense against infections most are large complex organic molecules (MW
>10,000), not normally found in the body
non innate, but adaptive: especially immunogenic:
foreign proteins
1. carefully targeted nucleic acids
some lipids
many large polysaccharides
! recognizes a specific foreign substance and
acts to immobilize or neutralize it but large simple molecules of many small repeating units (eg.
plastics) have little or no immunogenicity
2. amplifies the immune response, complement
reactions, etc against specific pathogen must be foreign to the host
3. is a systemic response our body is programmed to recognize our own

proteins as “self” ie. not immunogenic
effective throughout the entire body
but these same proteins may be strongly
4. Has memory immunogenic to others
protects you if you’re ever reinfected with same pathogen
eg. transfusions, transplants
resistance lasts a long time
microorganisms and pollen grains are immunogenic
Antigens because their surface membranes have many such
foreign molecules on them
any substance that can mobilize the immune system
examples of antigen containing structures:
! ie. provoke an immune response bacterial capsules
cell wall lipopolysaccharides of G- bacteria
can be free molecules or attached to cells of glycoproteins in cell membranes
bacteria, fungi, etc attachment sites for viruses
bacterial toxins and extracellular enzymes
the ability of a molecule to act as an antigen depends

small molecules such as peptides, nucleotides, and
many hormones are NOT immunogenic focus for the immunologic molecules and cells
!but may become so by attaching to the for viruses and other organisms that establish
body’s own proteins (=Haptens) themselves within body cells the immune system
uses a different process
eg. chemicals in poison ivy, animal dander,
some detergents, cosmetics, etc
the infected cells display major histocompatability
complex (MHC) molecules on their surface
actually, only certain parts of an entire antigen are
which bind to and display small peptides or
immunogenic
fragments of proteins that come from the
parasite
usually a small sequence of amino acids (~10)
that triggers an immune reactions
these MHC with foreign peptides form antigens
that can be recognized by antigen receptors
! = antigenic determinants (=epitopes)
on certain lymphocytes which identify and kill
infected cells, leaving healthy cells alone
most naturally occurring antigens have a variety of
antigenic determinants
The Immune Response
eg. large proteins have 100’s
The immune response (=specific immunity) involves
the interaction of two major processes in the
Antigen Processing
body, directed by two different kinds of
lymphocytes (WBC’s):
immune surveillance is a search for antigens
A. Antibody Mediated Immunity
uses a large population of white blood cells
(AMI; Humoral Immunity)
= lymphocytes
B. Cell Mediated Immunity
to control bacteria and large parasites immune system
(CMI;)
deploys soluble antigen receptors called antibodies
antibodies bind directly to parasite and provide a

Antibody Mediated Immunity ! produces numerous copies of identical cells with

identical antibodies on cell membranes
=AMI; =Humoral Immunity
c. differentiation into plasma cells and memory
Mediated by B lymphocytes (B-cells) cells
involves the release of proteins called antibodies plasma cells secrete antibodies
2,000 Ab/sec over few (4-5) days, then dies
B-Cell Development & Activation
memory cells do not secrete antibodies
1. by the time an infant is a few months old live for months or years
B lymphocytes (B cells) have completed the 1st
stage of their development: if later exposed to same antigen they can
develop into same kind of plasma cells and
manufactured in fetal liver secrete antibodies
they synthesize up to 100,000 antibody ie. they “remember” an earlier encounter with the
antigen
molecules that they hold in the cell
membrane Antibodies
2. The next stage of development occurs in lymph antibodies are proteins called immunoglobins
nodes and spleen and only occurs if B cell =gamma globulin of plasma proteins
encounters an antigen it recognizes:
each of us has ~ a billion different kinds of antibodies
a. specific B cells activated by exposure to an and each of these has a unique shape
antigen
each immunoglobin molecule consists of 4 polypeptide
!antigen binds to antibodies on cell chains joined together to form a “Y” shaped
membrane of B cell molecule
b. triggers clonal selection and multiplication each antibody has 2 or more combining sites
1st antibody released to blood by plasma cells
during primary response
! small concave areas at tip of arms of “Y” that attacks specific toxins eg. diptheria, tetanus,
are uniquely shaped and complementary to botulism toxin
the epitope blood group antibodies belong to this group
! cause agglutination
two long (=heavy, ~400 AA’s) chains and two short (=light, ~200
AA’s) chains linked by disulfide bonds Ig A
constant region ! same AA sequence for all in same class dimer
10-25% in serum
variable region ! =antigen binding sites (tips of Y) also found in body secretions:
mucus, saliva, urine, milk, tears
the body uses ~300 gene “pieces” to make >1 Billion different active against bacterial and viral infections
kinds of antibody molecules
inhibits attachment of parasites in gut
1st to encounter bacteria in GI tract
the amino acid sequence determines the specific passed to nursing child in mothers milk
shape of these polypeptide chains
Ig E
this unique shape allows a specific antibody to associated with allergies
causes certain WBC’s to release histamine
combine with specific antigen ! dilates capillaries
! constricts bronchi
Classes of Antibody Molecules:
Ig D
IgG very low concentrations in serum
most abundant antibody in plasma levels increase during chronic infections
75-80% of gamma globulin
also found in internal secretions formation of the antigen/antibody complex by B-cell
(synovial fluid, spinal fluid, peritoneal fluid)
effective against bacteria, viruses, and toxins
activity does not generally destroy the invader
plasma levels increase dramatically during
secondary responses ! it prepares it for destruction by
only Ig that can cross placenta non-specific phagocytosis (WBC’s)
triggering complement fixation
IgM CMI (T-cell activity)
largest of the antibodies
only found in blood
5-10% of plasma immunoglobins
antibodies bind to antigens to cause a variety of primary

! persons initial exposure to an antigen
possible effects: lag of several days before antibodies begin being
produced
1. Agglutination peak production in ~10 days
bind to antigens on cells to cause them to
clump together secondary
makes it easier for WBC’s to remove ! reexposure to same pathogen triggers memory cell
response
2. Precipitation memory cells can persist for 20 years or more
much quicker response
binds soluble antigens together causing them
much stronger response
to precipitate out of solution
makes it easier for WBC’s to remove them
Natural vs Artificial Immunity
3. Neutralization
binds to bacterial toxins (esp. exotoxins) and natural
causes them to be nontoxic ! immune response is triggered due to natural
exposure to a pathogen
4. Prevents viral attachment
artificial (=acquired)
binds to viral receptor sites to prevent viral
! immune response is triggered by a medical
invasion of cells
procedure, eg vaccination
(doesn’t work for latent viruses)
5. Stimulates Natural Killer Cells Active vs Passive Immunity

antibodies coat and mark a cell for destruction by the
NK cells active
=antibody dependent cell mediated cytotoxicity ! exposure triggers body’s own immune
response including memory cells
6. Complement Fixation
triggers complement reactions passive
especially against cellular antigens ! subject receives antibodies from another person or
cascade reactions can cause: animal, rather than making them himself
-cell lysis offers immediate protection, short term
-opsonization no active antibody production is stimulated
-inflammatory enhancement no memory develops
eg. fetus gets antibodies from mom

Primary vs Secondary Response eg. gamma globulin to treat hepatitis, botulism,
snake bites, etc
Cell Mediated Immunity
= CMI
Mediated by T lymphocytes (T-cells)
involves a more diverse group of cells than for AMI
usually, slower to respond
antigens are usually larger than in AMI
most active in:

bacterial infections
destruction of malignant tumor cells
transplant rejections
T-cells also contain antigen receptors on their cell

membranes
T-Cell Development & Activation
1. probably also first develop in fetal liver from stem

cells
2. then move to thymus where they develop and

proliferate
3. move into lymph nodes and spleen as T- cells
4. The next stage of development occurs only if T cell dampens activity of T and B cells
brings immune response to an end
encounters an antigen it recognizes:
iv. Delayed Hypersensitivity Cells
a. specific T cells activated by exposure to a
specific antigen (on a cell) chronic infections
cell mediated allergies
T-cells cannot recognize free antigens in the blood
generally need cell to cell contact to work
v. Memory Cells
eg. viral infected cell, cancer cell, bacterial cell
5. each T-cells secrete specific kinds of immunoactive
b. initiate clonal selection and multiplication of chemicals = cytokines (=lymphokines)
specific kind of T-cell
soluble chemical messengers by which cells of
c. differentiation into several cell types the immune system communicate with
each other
i. Helper T-cells (esp CD4 cells)
NOT antibodies
most prevalent of all kinds of T cells, 65%
directly helps T and B cells to function cytokines direct the activities of both B and
releases lymphokines:
! recruit lymphocytes T cells and phagocytes
! stimulate differentiation of lymphocytes
! help B cells recognize antigens Kinds of Cytokines
there can be no immune response without them
eg. chemotactic factor
ii. Cytotoxic T- cells (CD8 cells)
! attracts macrophages to invaders
directly kill specific target cells by lysis
especially effective against foreign cells, cancer cells, eg. macrophage activating factor
fungi , some protozoa and helminths
recognizes virally infected cells by viral antigens on ! tells macrophages to destroy antigen
cells surface gives them enhanced antibacterial activity:
increased metabolic activity
iii. Suppressor T-cells (CD8 cells) more lysosomes
increased phagocytosis
restricts rampant uncontrolled immune response
eg. lymphotoxin Interactions of AMI and CMI Systems:
! poison which kills any cell it contacts
requires direct cell contact both systems work together to increase the immune
response against specific foreign antigens
eg. migration inhibition factor
! halts macrophage migration eg. production of antibodies by B-cells often requires

helper T-cells
eg. Interleukin 1
esp. “T-dependent antigens” – proteins such as viruses, bacteria,
! stimulates helper T-cells in presence of antigen foreign RBC’s, hapten–carrier combinations
! attracts macrophages in inflammatory resonse eg. stimulate B-cells to differentiate into plasma cells
and produce antibodies
eg. Interleukin 2
! proliferation of TH cells
! proliferation and differentiation of B-cells
! activation of Tc and NK cells
eg. alpha interferon
! inhibits intracellular viral replication
! increases activity of macrophages against

microbes and tumor cells
eg. Tumor Necrosis Factor
! toxic to tumor cells
! enhances activity of phagocytic cells
eg. GM-CSF (Granulocyte Macrophage-Colony

Stimulating Factor)
! stimulates the formation of RBC’s and WBC’s

from stem cells
Neuroendocrine-Immune
eg. stress can activate parts of same pathway
Interactions
eg. mental state can influence the body’s resistance
all three systems are interconnected to disease: anxiety or psychological stress
increased severity of a cold
neural links:
hypothalamus! pituitary! adrenal! stress
neurons innervate immune system organs
such as spleen and lymph nodes >bld sugar ! reduced inflammatory response
chemical links: eg. immune system can be taught to react to visual

cue with an allergic reaction = conditioned
all three produce active chemicals response
neurotransmitters, hormones,
lymphokines
sometimes one chemical can have effect in all

three systems
all three coordinate and control the responses to the

outside world
the immune system acts as a “diffuse sense organ”
relays data about inflammation or infections to brain
Examples of interactions:
eg. Brain might respond to an infection by causing

fever and achy feeling (part of nonspecific
defense)
Effects of Aging on Immune System Clinical Applications of Immunity
reduced immune responsiveness: 1. Vaccinations
less red bone marrow and lymphatic tissue
loss of thymus ! lymphocytes fail to mature based on primary vs secondary response
fewer helper T cells and less responsive
fewer NK cells ! weaker surveillance primary
! persons initial exposure to an antigen

!infections become more common and more lag of several days before antibodies begin being
serious produced
peak production in ~10 days
epidemics have more severe impact on older secondary

population
! reexposure to same pathogen triggers memory cell
response
but number of autoantibodies increases with age memory cells can persist for 20 years or more
! more autoimmune diseases much quicker response
much stronger response
natural vs acquired immunity
natural
! immune response is triggered due to natural

exposure to a pathogen
acquired (=artificial)
! immune response is triggered by a medical

procedure, eg vaccination
active vs passive immunity
active
! exposure triggers body’s own immune

response including memory cells
Disorders of Immune System
passive most immune disorders can be categorized as:
! subject receives antibodies from another person or
1. autoimmune diseases
animal, rather than making them himself 2. hypersensitivities
3. immunodeficiencies
offers immediate protection, short term
no active antibody production is stimulated 1. Autoimmune Diseases
no memory develops 5% of adults in North America

eg. fetus gets antibodies from mom
! 2/3rd of victims are women
eg. gamma globulin to treat hepatitis, botulism, normal state of self tolerance breaks down due to:
snake bites, etc
! self reactive lymphocytes are normally

2. Monoclonal Antibodies
silenced during development
in this case some escape and attack body
specific B cell (with desired antibodies) is fused to
cancer cell
! new self antigens appear
due to gene mutation or hapten binding
! rapid production of large numbers of the
same antibody
! foreign antigens resembling self antigens
trigger antibodies that not only attack
3. Organ Transplants and Rejections
foreign antigens but self antigens as well
same principle as blood transfusions
autoantibodies & sensitized T-cells
usually need immunosuppressive drug therapy
some of most common autoimmune diseases:
eg. Multiple Sclerosis

destruction of myelin sheath of brain and
spinal cord
especially in young adults up to 50 million in US suffer from allergies
nerve fibers are severed
neurons short circuit 35.9 million (>70%) !hay fever
cycles of remission and relapse 10 million !allergic asthma
30,000 ! food allergies
eg. Myasthenia Gravis
best known of all human autoimmune diseases Ig E mistakes a harmless foreign substance for
destruction of neuromuscular junctions a dangerous invader and triggers runny
! Ach receptors
results in muscle weakness and fatiguability
nose, tears, itching, swelling
typical symptom = droopy eyelids
incidences of allergies are on the rise
eg. Graves Disease
increased thyroid activity some consider them a “disease of civilization”
! thyroid produces excessive amounts of
thyroxine
a. immediate (acute) hypersensitivity
mediated by B cells
eg. Juvenile Onset Diabetes Mellitis
destruction of beta cells in Islets of Pancreas IGE ! mast cells ! histamine
results in insulin deficiency may cause anaphylactic shock
eg. Rheumatoid Arthritis b. delayed hypersensitivities

joint inflammation and destruction eg. poison ivy
eg. Lupus mediated by T cells

a group of diseases
arthritis and dermatitis are most common manifestations
antihistamines don’t work
attacks kidneys, heart, lungs, skin use corticosteroids
eg. Narcolepsy 3. Immunodeficiencies

seems to have an autoimmune origin
failure of immune system to respond adequately
2. Hypersensitivities to a pathogen
eg. allergies eg. SCID (Severe Combined Immunodeficiency Disease)

congenital
born without functional immune system
eg. AIDS (Acquired Immunodeficiency Syndrome)

results from infection with HIV virus
usually acquired by sexual contact or drug
injections
HIV targets helper-T (CD4) cells
Human Anatomy & Physiology: Body Defense & Immunity; Ziser Lecture Notes, 2014.4 39

Body Defenses & Immunity: But If Skin Is Moist, Not Cleaned Frequently Enough

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Body Defenses & Immunity

the immune system is a functional system rather

Many factors not directly related to our “immune 1. Nonspecific Immunity

eg. Age: mainly an immune response

The Immune System

Nonspecific Immunity a. consists of multiple layers of tightly packed

Physical Barriers e. skin also contains bacteriocidal chemicals

1. Intact Skin 2. Mucous Membranes

(‘ciliary escalator’ ! 1-3 cm/hr) h. vaginal secretions

especially bacteria takes 10-30 minutes to kill most bacteria

mechanism of phagocytosis: eg. Staph and Actinobacillus actually produce

5. Inflammatory Response blood vessels dilate in area of damage

from localized area causes swelling (edema), redness and heat

sometimes loss of function b. Phagocyte Migration and Phagocytosis

chemical attractants, eg. kinins, draw WBC’s to site

c. repairs or replaces damaged tissues as WBC’s die ! pus accumulates

occurs in three major stages: c. Tissue Repair

b. phagocyte migration and phagocytosis 6. Fever

c. tissue repair systemic rather than local response

fever symptoms: they can operate nonspecifically or specifically

slight increase in temperature: trigger a cascade reaction (inactive! active)

!digests a hole in bacterial cell, killing it

8. Interferon might work better with other agents in combination

antiviral chemical secreted by infected cells

they are host cell specific, not virus specific

! different tissues in same host produce

all interferons are small proteins

produced by infected cells and spread to

Specific Immunity on its size and complexity

3. is a systemic response our body is programmed to recognize our own

the ability of a molecule to act as an antigen depends

antibodies bind directly to parasite and provide a

Antibody Mediated Immunity ! produces numerous copies of identical cells with

antibodies bind to antigens to cause a variety of primary

5. Stimulates Natural Killer Cells Active vs Passive Immunity

eg. fetus gets antibodies from mom

Mediated by T lymphocytes (T-cells)

involves a more diverse group of cells than for AMI

usually, slower to respond

antigens are usually larger than in AMI

most active in:

T-cells also contain antigen receptors on their cell

T-Cell Development & Activation

1. probably also first develop in fetal liver from stem

2. then move to thymus where they develop and

3. move into lymph nodes and spleen as T- cells

! halts macrophage migration eg. production of antibodies by B-cells often requires

! proliferation and differentiation of B-cells

! activation of Tc and NK cells

eg. alpha interferon

! inhibits intracellular viral replication

! increases activity of macrophages against

eg. Tumor Necrosis Factor

! toxic to tumor cells

! enhances activity of phagocytic cells

eg. GM-CSF (Granulocyte Macrophage-Colony

! stimulates the formation of RBC’s and WBC’s

chemical links: eg. immune system can be taught to react to visual

sometimes one chemical can have effect in all

all three coordinate and control the responses to the

the immune system acts as a “diffuse sense organ”

relays data about inflammation or infections to brain

eg. Brain might respond to an infection by causing